MMP7 (Matrix metallopeptidase 7)

Our study delineates CAF heterogeneity in CRC and highlights the CTHRC1+ CAF subtype as a critical organizer of an immunosuppressive niche. The THBS2-SDC4 signaling pathway between CTHRC1+ CAFs and MMP7+ epithelial cells acts as a potential therapeutic target to disrupt protumorigenic crosstalk and improve clinical outcomes for CRC patients.

P=N/A, N=300, Recruiting, Children's Hospital of Fudan University | Trial completion date: Dec 2026 --> Dec 2028 | Trial primary completion date: Mar 2026 --> Dec 2028

Conclusions Overall, the disrupted ADMA-SDMA balance and Ca++ permeability impair the regulation of claudin-4, MMP-7, and PD1/PD-L1 in GC patients. These variables hold promise as diagnostic and therapeutic targets for improved GC management.

Consistent with these in silico findings, exposure of mice to 24 μg/kg TCDF significantly increased the expression of Mmp7 and Hsp90aa1 in murine colonic tissues, increased the levels of proinflammatory cytokines Ifn-γ, Il-1β, and Il-6, and downregulated the expression of Mucin 2 (MUC2). Connectivity Map analysis based on the PCDD/F-related gene signature identified five candidate compounds targeting MMP7 and HSP90AA1, of which four HSP90 inhibitors (tanespimycin, alvespimycin, NVP-AUY922 and AT-13387) showed negative connectivity scores, suggesting potential to reverse the pollutant-induced expression profile.

Increases in MMP-2 and MMP-9 in response to estrogen and progesterone promote placentation, uteroplacental vascularization and fetal growth during healthy pregnancy, but are altered in preeclampsia (PE)...Understanding the aberrant uteroplacental and vascular signaling and remodeling by MMPs could help design new biomarkers and remedies for PE. Targeting bioactive factors and rectifying MMP imbalance could improve vascular and uteroplacental remodeling, and manage HTN-Preg, FGR and PE.

This review also discusses how ECM composition and structure are altered in the tumor microenvironment (TME), thereby preventing cell interactions and promoting cancer growth. Finally, it compiles the existing studies to anticipate a future era in which MMPs could serve as effective prognostic biomarkers and potential treatment targets for RCC, with implications for improving diagnostic and therapeutic interventions targeting ECM remodeling to suppress cancer progression.

Time-lagged analysis demonstrated that 90% of the identified cancer-associated proteins are markers for long-term cancer risk, with observed associations more than 5 years pre-diagnosis after multiple-testing correction. These findings underscore the potential of circulating proteomic markers beyond known risk factors for elucidating etiologic mechanisms and improving risk stratification across cancers.

This comprehensive transcriptomic study unveils the molecular complexity underlying GERD-to-Barrett's esophagus progression, identifying key genes and pathways that drive pathological transformation.

P=N/A, N=14, Completed, University of Virginia | Active, not recruiting --> Completed | N=100 --> 14

In a physiologically relevant, cancer-associated fibroblast (CAF)-enriched xenograft model, MMP2-engineered CAR-T cells displayed increased intratumoral accumulation and durable tumor control. These findings establish MMP2-based single-enzyme ECM remodeling as a simple, scalable, and clinically translatable strategy to overcome stromal resistance and advance CAR-T therapy for solid tumors.

DKA causes a unique inflammatory pattern distinct from inflammatory changes in acute hyperglycemia or T1D-related autoimmunity. Alterations in MMPs and their tissue inhibitors play a dominant role in this inflammatory profile.

P=N/A, N=7, Terminated, University of Arizona | N=20 --> 7 | Active, not recruiting --> Terminated; Lack of enrollment